30 September 2016 : Clinical Research
High-Level Expression of Toll-Like Receptors on Dendritic Cells in Adult Patients with Burns on ≥90% of Total Body Surface Area (TBSA)
Xu ZhangBD, Na LiACE, Yan MengAD, Renjing ZhangBD, Jinjun BianC, Ying YaoBC, Jinbao LiFG, Xiaoming DengFDOI: 10.12659/MSM.897433
Med Sci Monit 2016; 22:3493-3499
Abstract
BACKGROUND: As a serious clinical problem, severe burn injury disturbs the immune system, resulting in progressive suppression of immune response. TLRs are associated with immune system activation, but the effect of TLRs levels on circulating cDCs of severe burn injury patients has not been fully assessed.
MATERIAL AND METHODS: Ten patients with total body surface area (TBSA) burned >90% admitted to our institution were enrolled in this study. We analyzed TLR2, TLR4, and TLR9 expression on the circulating cDCs by using multicolor flow cytometric analysis in patients at 14 days to 28 days after burn injury according to mortality, and We also assessed Demographics, clinical outcomes, organ function, and inflammatory and acute-phase responses.
RESULTS: No difference in TBSA, sex, age, or number of operations before the first 14 days after injury were observed between surviving and non-surviving burn patients. The levels of TLR2, TLR4, and TLR9 in circulating cDCs were significantly and consistently elevated in all patients compared to age-matched healthy volunteers, and survivors exhibited higher TLR2 and TLR4 values than non-survivors. Of the survivors, TLR2 and TLR4 levels were higher at 28 days than at 14 days after injury, while the difference in TLR9 levels was not significant. TLR2 levels of non-survivors at 28 days after injury decreased, and the TLR4 and TLR9 levels showed no significant difference.
CONCLUSIONS: TLRs levels in circulating cDCs are highly activated in severe burn injury patients up to 28 days after injury. The low expression of TLR2 in cDCs may be useful as a potential marker predicting the poor prognosis of severe burn patients.
Keywords: Burns, HLA-DR Antigens, Systemic Inflammatory Response Syndrome, Toll-Like Receptors
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